PubMed Health⌕ Search

Biomedical subjects

B K Armstrong

Publications and source records attributed to B K Armstrong.

At least 19 recordsLinked to original sources
PubMed1995

Risk of cutaneous melanoma associated with pigmentation characteristics and freckling: systematic overview of 10 case-control studies. The International Melanoma Analysis Group (IMAGE).

Using individual subject data from 10 case-control studies, comprising over 3000 cases and almost 4000 controls, we have estimated the relative risk of melanoma associated with aspects of complexion, namely, hair, eye and skin colour and freckling in adulthood, and have examined the relationships between these factors and naevus count in terms of melanoma risk. Compared with individuals with black or dark brown hair, the relative risks for developing melanoma in those with light brown, blonde and red hair were 1.49 (95% CI 1.31, 1.70), 1.84 (95% CI 1.54, 2.21) and 2.38 (95% CI 1.90, 2.97), respectively. Individuals with blue eyes had a risk 1.55 (95% CI 1.35, 1.78) times that for those with brown eyes, or 1.15 (95% CI 0.94, 1.40) after adjusting for hair colour and freckling in adulthood. The relative risks associated with hair and eye colour were independent of those for naevus count and skin colour. Light skin colour and high freckle density were also highly significant risk factors, independent of each other and of naevus count and hair and eye colour. The risks associated with these factors, while individually modest, are largely independent, and thus pigmentation characteristics and freckling tendency should be useful in identifying high risk groups to be targeted for prevention.

Case-Control Studies↗
PubMed1995

Risk of cutaneous melanoma associated with a family history of the disease. The International Melanoma Analysis Group (IMAGE).

In a combined analysis of 2952 melanoma patients and 3618 controls from 8 case-control studies in white populations the risk of cutaneous melanoma was 2.24-fold higher (95% CI, 1.76-2.86) in subjects who reported at least one affected first-degree relative than in subjects who did not. There was no evidence for heterogeneity in the relative risk between the studies, which were from a wide range of latitudes and hence degrees of sun exposure. The effect of family history on melanoma risk was independent of age, naevus count, hair and eye colour, and freckling. There was no evidence for a relationship between family history and primary site of melanoma but there was some suggestion that the familial patients were more likely to have superficial spreading melanoma or lentigo maligna melanoma than acral lentiginous melanoma or nodular melanoma.

Case-Control Studies↗
PubMed1995

A dose-response curve for sun exposure and basal cell carcinoma.

A population-based case-control study of sun exposure and basal cell carcinoma (BCC) was conducted in Western Australia in 1988. Its aim was to examine the relationship between risk of BCC and the amount and pattern of sun exposure. This report deals with amount of exposure. The odds ratios (ORs) for BCC on the head and neck and limbs decreased with increasing total exposure, whereas the opposite was observed for BCC on the less heavily exposed trunk, with the highest OR in those with the greatest exposure. In an analysis of all body sites together in which the total hours of exposure to the specific site was treated as a continuous variable, an initial rise in risk of BCC was seen with a peak OR of 1.4 at about 35,000 hr of exposure, followed by a fall. In contrast to these site-specific patterns, lifetime accumulated sun exposure of the whole body showed no appreciable association with BCC either in total or for working days only. Risk of BCC was positively associated with lifetime exposure on non-working days, however, with an OR for higher than baseline categories of around 1.7. There was a significant interaction between ability to tan and total and occupational sun exposure. Risk increased with increasing exposure in those who tanned well but not in those who tanned poorly. This pattern is consistent with other observations which indicate that beyond a certain level of sun exposure risk of BCC does not increase further.

Adult↗
PubMed1995

Does intermittent sun exposure cause basal cell carcinoma? a case-control study in Western Australia.

Our report deals with the relationship of pattern and timing of sun exposure to basal cell carcinoma (BCC) in a population-based case-control study conducted in Western Australia in 1988. The main measure of intermittent exposure was based on the amount of exposure on non-working days relative to that over the whole week. Outdoor recreational activities, holidays and sunburn were also considered to be markers of intermittent exposure. We observed a statistically significant increase in risk of BCC with increasing proportion of weekly sun exposure obtained at the weekend, especially in late teenage (OR = 3.9, 95% CI 1.9-7.8 for maximum intermittency of exposure), exposure of the site of skin cancer during holidays (OR = 1.9, 95% CI 1.1-3.1 for the highest exposure quarter) and sunburn to the site (ORs of 1.8 for 3-10 and 1.5 for 11+ sunburns in a lifetime). Risk of BCC increased substantially with increasing intermittency in poor tanners but not at all in good tanners. Our data suggest that a particular amount of sun exposure delivered in infrequent, probably intense increments will increase risk of BCC more than a similar dose delivered more continuously over the same total period of time.

Adult↗
PubMed1995

Skin cancer.

It is estimated that 92,000 new cases of melanoma and 2,750,000 cases of nonmelanocytic skin cancer occur worldwide each year. Incidence of these cancers varies more than 100-fold from low rates in Asian populations to very high rates in the white population of Australia. Incidence of melanoma has been increasing in white populations by some 3% to 7% per year over the past 30 years; recent very sharp increases in some populations are probably due to early and increasing detection of cancers that were already there. Incidence of nonmelanocytic skin cancers probably is also increasing. Sun exposure is the main cause of skin cancer, accounting for at least 65% of melanomas worldwide and a much higher proportion in white populations. Pattern as well as amount of sun exposure is important in determining the risk of melanoma and probably also of basal cell carcinoma, with an intermittent pattern being associated with the greatest risk. There is increasing evidence that nonsolar sources of ultraviolet radiation, in particular sunlamps and sunbeds, increase the risk of melanoma, and PUVA therapy and exposure to ionizing radiation are established causes of nonmelanocytic skin cancer.

Female↗
PubMed1995

Effects of low doses and low dose rates of external ionizing radiation: cancer mortality among nuclear industry workers in three countries.

Studies of the mortality among nuclear industry workforces have been carried out, and nationally combined analyses performed, in the U.S., the UK and Canada. This paper presents the results of internationally combined analyses of mortality data on 95,673 workers (85.4% men) monitored for external exposure to ionizing radiation and employed for 6 months or longer in the nuclear industry of one of the three countries. These analyses were undertaken to obtain a more precise direct assessment of the carcinogenic effects of protracted low-level exposure to external, predominantly gamma, radiation. The combination of the data from the various studies increases the power to study associations between radiation and specific cancers. The combined analyses covered a total of 2,124,526 person-years (PY) at risk and 15,825 deaths, 3,976 of which were due to cancer. There was no evidence of an association between radiation dose and mortality from all causes or from all cancers. Mortality from leukemia, excluding chronic lymphocytic leukemia (CLL)--the cause of death most strongly and consistently related to radiation dose in studies of atomic bomb survivors and other populations exposed at high dose rates--was significantly associated with cumulative external radiation dose (one-sided P value = 0.046; 119 deaths). Among the 31 other specific types of cancer studied, a significant association was observed only for multiple myeloma (one-sided P value = 0.037; 44 deaths), and this was attributable primarily to the associations reported previously between this disease and radiation dose in the Hanford (U.S.) and Sellafield (UK) cohorts. The excess relative risk (ERR) estimates for all cancers excluding leukemia, and leukemia excluding CLL, the two main groupings of causes of death for which risk estimates have been derived from studies of atomic bomb survivors, were -0.07 per Sv [90% confidence interval (CI): -0.4, 0.3] and 2.18 per Sv (90% CI: 0.1, 5.7), respectively. These values correspond to a relative risk of 0.99 for all cancers excluding leukemia and 1.22 for leukemia excluding CLL for a cumulative protracted dose of 100 mSv compared to 0 mSv. These estimates, which did not differ significantly across cohorts or between men and women, are the most comprehensive and precise direct estimates of cancer risk associated with low-dose protracted exposures obtained to date. Although they are lower than the linear estimates obtained from studies of atomic bomb survivors, they are compatible with a range of possibilities, from a reduction of risk at low doses, to risks twice those on which current radiation protection recommendations are based.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1994

DNA repair capacity as a risk factor for non-melanocytic skin cancer--a molecular epidemiological study.

Capacity to repair UV-induced DNA damage was studied by use of host cell reactivation assay in T lymphocytes isolated from 86 cases and 87 controls (aged 44-68 years) who were participants in a population-based case-control study of basal cell (BCC) or squamous cell (SCC) carcinoma of the skin in Geraldton, Western Australia. Lymphocytes were cultured and transfected with either control or UV-irradiated plasmids (254 nm, 350 J/m2) containing a reporter gene [the chloramphenicol-acetyltransferase (CAT) gene], and the repair capacity was determined by measuring CAT gene expression in protein extracts prepared from the transfected cells. DNA repair activity was 1.07 (95% confidence interval 0.94-1.26) times greater in BCC cases than in controls for each 350 J/m2 increment in UV dose to the plasmids, and 1.04 (95% confidence interval 0.85-1.26) times greater in SCC cases than in controls, though the differences were not statistically significant. DNA repair activity showed little association with age, sex and viability of the lymphocytes, though it was positively associated with their blastogenic rate (p = 0.055).

Adult↗
PubMed1994

Melanocytic nevi in children. I. Anatomic sites and demographic and host factors.

A survey of benign melanocytic nevi was conducted among schoolchildren in Perth, Western Australia, in 1985, with the aim of describing the prevalence and causes of nevi. Children were recruited from Perth public schools that were chosen to be representative of the socioeconomic and geographic distribution of the population. Of 4,898 eligible children, 2,595 (53%) had all of their nevi counted by one member of a team of five nurses. Analysis was restricted to 2,552 children aged 5-14 years. Children of European origin (i.e., white children), who comprised the majority of the sample (2,376 children), had many more nevi than did children of other ethnic origins. Among white children, the prevalence of nevi increased progressively with age, although the number of nevi per unit of skin area reached a plateau at about 9 years of age. Boys had more nevi at all ages than did girls. The number of nevi per unit of area was highest on the lateral surfaces of the upper limbs and the face and neck, and was lowest on the lower limbs. Children whose parents had been born in Southern Europe were likely to have few nevi. Children with red hair had relatively few nevi, but children with light skin generally had more nevi than children with darker skin. Ability to tan and propensity to burn were also associated with number of nevi, although not in a simple fashion; numbers of nevi were highest in intermediate categories of these two variables. The relation with freckling was also complex; the mean number of nevi increased with increasing freckling until the freckling became moderate to heavy, after which it fell.

Adolescent↗
PubMed1994

Melanocytic nevi in children. II. Observer variation in counting nevi.

A survey of benign melanocytic nevi was conducted among children in Perth, Western Australia, in 1985. Children were examined by one of a team of five nurses who counted all of their nevi. Linear regression was performed on the logarithmically transformed mole counts to assess the degree of interobserver variation. Among 2,354 white children aged 5-14 years, 3.9% of the variation in numbers of nevi of all sizes and 7.7% of the variation in nevi 2 mm or more in diameter was attributed to variation among observers. The observer variation was less for the back than for any other body site. Differences between observers were greater in children with heavy freckling than in children with little or no freckling. However, the interaction between degree of freckling and observer accounted for more than 1% of the variation in counts only at sites where freckling was common (the face and neck and the upper limbs). The reproducibility of counts made by pairs of observers on 236 of the children, estimated by intraclass correlation coefficients, was 0.79 for all nevi and 0.65 for nevi 2 mm or more in diameter. The mean count of nevi on the back obtained by examining photographs of 100 children aged 8-9 years (11.9 nevi) was similar to that recorded by the examiners (12.3; p = 0.31), and the two measures were highly correlated (r = 0.89).

Adolescent↗
PubMed1994

UV and skin cancer: specific p53 gene mutation in normal skin as a biologically relevant exposure measurement.

Many human skin tumors contain mutated p53 genes that probably result from UV exposure. To investigate the link between UV exposure and p53 gene mutation, we developed two methods to detect presumptive UV-specific p53 gene mutations in UV-exposed normal skin. The methods are based on mutant allele-specific PCRs and ligase chain reactions and designed to detect CC to TT mutations at codons 245 and 247/248, using 10 micrograms of DNA samples. These specific mutations in the p53 gene have been reported in skin tumors. CC to TT mutations in the p53 gene were detected in cultured human skin cells only after UV irradiation, and the mutation frequency increased with increasing UV dose. Seventeen of 23 samples of normal skin from sun-exposed sites (74%) on Australian skin cancer patients contained CC to TT mutations in one or both of codons 245 and 247/248 of the p53 gene, and only 1 of 20 samples from non-sun-exposed sites (5%) harbored the mutation. None of 15 biopsies of normal skin from non-sun-exposed or intermittently exposed sites on volunteers living in France carried such mutations. Our results suggest that specific p53 gene mutations associated with human skin cancer are induced in normal skin by solar UV radiation. Measurement of these mutations may be useful as a biologically relevant measure of UV exposure in humans and as a possible predictor of risk for skin cancer.

Adult↗
PubMed1994

Sun exposure and non-melanocytic skin cancer.

Non-melanocytic skin cancer has long been regarded as one of the harmful effects of solar ultraviolet (UV) radiation on human health. In this review, we examine epidemiologic evidence linking sun exposure and skin cancer coming from both descriptive studies in populations and analytical studies involving estimates of exposure in individuals. Particular attention is given to the quality of the published data. The epidemiologic evidence that sun exposure causes skin cancer is mainly indirect. Incidence or mortality is inversely related to latitude in populations of mainly European origin (e.g., the United States, Australia), and is higher in people born in Australia (high ambient solar radiation) than in migrants to Australia from the United Kingdom (lower ambient radiation). Skin cancer occurs mainly at sun-exposed body sites and in people who are sensitive to the sun; a reduced capacity to repair UV-induced DNA damage appears to increase the risk. The direct evidence linking sun exposure and skin cancer is weaker with few well-conducted studies of sun exposure in individuals. Mostly, studies of total sun exposure have not found statistically significant positive associations; those that did, had not adjusted for potential confounding by age and gender and thus their interpretation is limited. Studies of occupational sun exposure had relative risks not greater than 2.0; recreational exposure has been little studied. Other measurements, less direct but potentially less prone to measurement error, are sunburn (not evidently associated with skin cancer risk) and indicators of benign cutaneous sun-damage (strongly associated but lacking empirical evidence that sun exposure is their main cause). Many questions remain about the relationship between sun exposure and skin cancer.

Adult↗
PubMed1994

Stratospheric ozone and health.

BACKGROUND: Stratospheric ozone is being depleted and ambient ultraviolet (UV) irradiance is probably increasing. While remedial steps have been taken through the Montreal protocols, at best it will take some 90 years for stratospheric ozone concentrations to return to the levels existing in the 1970s. METHODS: The evidence that these changes may have harmful effects on health has been reviewed. RESULTS: The direct harmful effects are skin cancer, ocular damage and, possibly, immune suppression with an increase in infectious disease. Indirect, harmful effects resulting from climate change, changes in atmospheric chemistry, and changes in food supply may also occur. Beneficial effects are also possible but have largely escaped attention. Quantification of these effects is either uncertain or impossible at present and the outcomes for health in 50 years time can only be guessed at. CONCLUSIONS: To understand better the health consequence of stratospheric ozone depletion, we need to know the quantitative relationship between ambient UV radiation and skin cancer, whether or not UV radiation really causes cataract and other ocular effects and what the quantitative relationships are, whether effects of UV radiation on immune function produce detectable health consequences, whether there are important beneficial effects of increasing UV radiation and, ultimately, what the balance of all these effects might be on health on a global scale.

Atmosphere↗
PubMed1994

Recent incidence trends imply a nonmetastasizing form of invasive melanoma.

In the mid- to late-1980s white populations in Australia, New Zealand and Scotland showed a sharp increase in melanoma incidence above preceding long-term trends, in some cases as much as doubling in as little as 2 years. Most of this increase was in thin melanomas, (< 1.50 mm thick), and males were more affected than females. Thicker melanomas also generally increased in incidence, particularly in males aged 65 years or older. Examination of Australian Medicare and pathology laboratory data indicated that excision of skin lesions and laboratory diagnosis of pigmented lesions also rose sharply in this period, suggesting that advancement of the time of diagnosis was a likely factor in the increase in melanoma incidence. However the maintenance of new higher incidence levels and the increase in incidence of thicker lesions suggests that advancement of diagnosis cannot explain all of the increase. A real increase in incidence and increasing diagnosis of a preexisting, non-metastasizing form of thin melanoma may also have contributed.

Adolescent↗
PubMed1994

Seven-year follow-up of a smoking-prevention program for children.

Smoking-prevention programs, run by both teachers, and teachers and peers, have been introduced into school curricula in many parts of the world. This paper describes a long-term follow-up of a randomised controlled trial of a smoking education program for children conducted in Western Australia. Seven years after the first survey of 2,366 Year 7 students in 1981, 68 per cent of initial participants were traced through public records; 53 per cent of these responded to a new survey concerning smoking. Previous follow-up after one and two years had shown that both teacher-led and peer-led programs continued to reduce the taking up of smoking by girls to about the same degree, whereas in boys, the teacher-led program appeared to be effective after one year but neither program was effective after two years. In nonsmoking girls, both the intervention programs maintained their effects at the seven-year follow-up, with an almost 50 per cent reduction in smoking prevalence in the intervention group. Nonsmoking girls appeared to respond to cigarette advertisements. Mothers seemed to influence nonsmokers of both sexes and brothers seemed to influence smokers of both sexes. The seven-year follow-up confirmed the results seen at two years for boys, that the effects of the education program had dissipated. However, this study suggests that the smoking-prevention program had a lasting effect on preventing girls from taking up smoking.

Adolescent↗
PubMed1994

Cutaneous melanoma.

Between the early 1960s and the late 1980s, the incidence of melanoma increased at a rate of 3-7% per year in populations of mainly European origin. Corresponding trends were observed in mortality. Higher rates of increase in incidence were observed in a few populations (eg 8.9% per year in Hawaii whites). With the exception of Japan and possibly Puerto Rico, incidence rates of melanoma have remained stable in the few populations of mainly non-European origin for which reliable incidence data were available. A comparison of age specific trends in incidence and mortality in populations of mainly European origin showed two general patterns: a continuous increase in incidence in all age groups but with moderation or cessation of the previous rising trend in mortality in younger people in more recent time periods (eg Canada, continental USA, Denmark and the UK) and recent moderation or cessation of both incidence and mortality trends in younger people (eg New Zealand and, possibly, Hawaii whites). The first of these two patterns appeared to be the most common. Studies of site specific trends in incidence in 13 populations indicate that the highest rates of increase have generally been for melanomas on the trunk and the lowest for those on the head and neck. There is weak evidence to suggest that the rate of increase on the lower limbs has been greater in women than in men. Studies of incidence trends in the 1980s by thickness of melanoma in seven populations show that relative and absolute incidence has increased most for the thinnest melanomas and least for the thickest lesions. Increasing detection, earlier diagnosis and a real rise may together explain the increase in incidence of melanoma. The increases in mortality suggest that incidence has really increased, and the recent moderation in mortality trends may be explained by improved survival from melanoma due, most likely, to increasingly early diagnosis. In some populations, it may also indicate that the incidence increases are coming to an end. The disproportionately increasing incidence of thin melanoma, the divergence between incidence and mortality trends and the recent sharp increases in incidence in some populations suggest that earlier diagnosis or greater detection of less aggressive melanomas may have contributed to the incidence trends. A progressive change from predominantly occupational to predominantly recreational patterns of sun exposure is the most likely cause of increasing real incidence of melanoma in populations of mainly European origin.

Adolescent↗
PubMed1993

An analysis of a melanoma epidemic.

Between 1986 and 1988 the annual incidence of invasive melanoma in the Hunter area of New South Wales, Australia, almost doubled to 52.5 per 100,000 in men and 42.9 per 100,000 in women. These rates have been maintained and are similar to those reported for 1987 in Queensland, Australia, which are the highest in the world. Most of the increase in incidence was in melanomas less than 1.50 mm in thickness, and adults of both sexes and all ages were affected. Thicker melanomas also increased in incidence but only in adults 45 years and older, and mainly in men. An analysis of health insurance data on treatment of skin lesions and data from a histopathology laboratory suggested that diagnosis and treatment of skin lesions generally in the Hunter area had increased almost 2-fold over this period. Advancement of the time of diagnosis and a real increase in incidence were likely explanations for some of the observed trends. Increasing diagnosis of a non-metastasising form of thin melanoma, consequent upon increasing removal of pigmented skin lesions by medical practitioners, may also explain some of the observed increase in the incidence of the disease. This possibility has important implications for proposed population screening programs, and methods are needed to distinguish such lesions, if they exist, from potentially fatal melanoma.

Adult↗
PubMed1993

How much melanoma is caused by sun exposure?

Estimates have been made of the proportion of cutaneous malignant melanomas caused by sun exposure by comparing the observed incidence of melanoma with estimates of the incidence in the absence of sun exposure. The estimated proportions varied from 0.97 in males and 0.96 in females in Queensland, Australia, when the incidence on the whole body was compared with that on unexposed sites, to 0.68 when incidence in people born in Australia was compared with that in migrants to Australia from areas of lower sun exposure. A comparison of US Whites and US Blacks, in which the incidence in Blacks was taken as the incidence in unexposed Whites, gave estimates of 0.96 in males and 0.92 in females. It was estimated that some 59,000 (65%) of about 92,000 melanomas that occurred worldwide in 1985 were caused by sun exposure. This is probably a minimum estimate. That 20% of the world's melanomas are estimated to occur in Black African and Asian populations and are of unknown cause would justify studies of the causes of melanoma in these populations.

Algorithms↗